Abstract

Publisher Summary Recently, electrophysiologic studies have suggested that the arrhythmias leading to sudden cardiac death may have a different mechanism and pathophysiology from those producing frequent premature ventricular contractions. This has led to the speculation that agents that affect the duration of the action potential and His-Purkinje and ventricular muscle refractoriness by blocking potassium channels may alter the sudden cardiac death syndrome. A number of new agents that are known to block potassium channels in these tissues have recently commenced basic and clinical studies. All evidence available at this time suggests the need for new antiarrhythmic compounds with improved or different mechanisms of action to combat the frequency of symptomatic cardiac arrhythmias, and the mortality that results from the more refractive forms. This chapter presents the pharmacology and chemistry of existing and new antiarrhythmic drugs, together with pharmacokinetic and pharmacodynamic actions of the drugs. Particular emphasis on the interaction of these antiarrhythmic drugs with other cardiac and noncardiac drugs and in disease states is made.

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